Effects of Mercury on Neurological Development


Section A:  Neurological effects of mercury at relatively typical environmental levels


Section B:  Special vulnerability of infants to effects of mercury during the early postnatal period

Section C:  Specifics about neurological harm caused by mercury, especially as related to autism


Section DAlternative types of infant nutrition, with different concentrations of mercury


Section E:  Other questions about effects of mercury exposure in the early postnatal period


 Section F:  Long-term, latent effects of mercury exposure


 Appendix:  More evidence about effects of Methylmercury



Section A:  Neurological effects of mercury at relatively typical environmental levels:


 According to a publication of the National Scientific Council on the Developing Child, on a Harvard University website, At levels frequently measured in our environment, heavy metals (which include mercury) interfere with the construction of the basic framework of the maturing brain as well as with its function. These toxic effects include disruption of neural cell migration from one part of the brain to another, as well as the formation of synapses….”1   See Figure 1 later for indication that a very large part of the maturing of the human brain takes place during the first year after birth.  Some neural cell migration and most formation of synapses takes place after birth.1a


Lead is one of the heavy metals that is well known for its neurodevelopmental toxicity, but mercury is another one whose toxicity is also well established.  One especially harmful form of mercury, methylmercury, is present in significant concentrations in the typical human body, mainly as a result of consumption of fish and seafood that contain it.2  Long-term, low-dose exposure to methylmercury stemming from maternal consumption of fish and seafood is recognized as neurodevelopmentally toxic to the fetus/infant.3  Strong basis for that belief is reflected in a 2010 systematic review of 48 articles about studies conducted in the U.S. and four other countries,4 and in other studies as well.5  Developmental neurotoxicity of organic mercury (which includes methylmercury) “has been observed at very low exposure levels,” according to the U.S. Agency for Toxic Substances and Disease Registry (ATSDR).6  


(Methyl/organic mercury:  According to 2003 data from the U.S. National Center for Health Statistics, among the many women who have total blood mercury levels exceeding the safe level established by the EPA (5.8 mcg/L), over 90% of the total mercury was found to be “organic/methyl mercury.” (authors of a study on the topic considered organic mercury to be basically methyl)6a   And it is a substantial number of newborns (over 300,000 per year in the U.S. alone) who are affected by maternal mercury levels exceeding the EPA’s safe threshold.6b)


At least eight published studies have found high levels of mercury in those with ASD (autism spectrum disorders).7  A 2007 study determined the level of mercury, lead, and zinc in baby teeth of children with autism spectrum disorder and found that children with autism had significantly (2.1-fold) higher levels of mercury but similar levels of lead and zinc.7b  As the authors noted, baby teeth are a good measure of cumulative exposure to toxic metals during early infancy; this is consistent with the fact that most babies sprout their first tooth sometime between 4 and 7 months of age.7c 


A 2013 study, by a team of 12 researchers, found severity of all basic characteristics of ASD to vary in proportion to levels of mercury in the affected children, aged 5 to 16.7a    Other toxic metals were also implicated, but mercury was the only metal that was “the most consistently significant variable” in both whole blood and red blood cells. The p-value was .0003, indicating three chances out of 10,000 that this relationship was a random occurrence.  (Bear in mind that a dose-response relationship, such as was found in this study, is considered to be especially strong evidence of a causal relationship.)


There is additional evidence that typical exposures of infants to mercury are at hazardous levels:  The maximum mercury concentration allowed in bottled water, according to U.S. Federal Regulations, is 2 ppb (parts per billion).8  In contrast with that, the U.S.  ATSDR, based on the available information from various countries of the world, estimated that the mean concentration of mercury in breast milk of non-exposed women is 8 ppb.9  Notice that this figure applied to women without unusual exposure to mercury; it is important to bear in mind that large numbers of people in the general population are in the more-exposed category, including many people working with art materials, some who work in dental offices, recycling facilities or laboratories, those with large numbers of dental amalgam fillings, those who live or work in buildings painted on the inside with mercury-containing latex paints or who use certain cosmetics, and many who live or work near or downwind from coal-burning power plants, municipal or medical incinerators, or waste disposal sites; mercury is also present in vehicle emissions, especially in diesel emissions,10 which is very significant in that a major 2013 study found that autism prevalence correlates closely with geographic locations where diesel emissions are known to be high.11, and two California studies have found autism to be increased near freeways.  


The major variations in infants’ typical exposures to this toxin, with greatly varying consequences for infant development, is illustrated by the following quotation from a review article: “Among women who eat a lot of fish,…levels of mercury in breast milk may exceed levels in unexposed women by 100-fold.”(12)


The ongoing nature of human exposure to mercury is indicated in a report published in late 2012 by a Dartmouth College group, which states, “methylmercury in commonly consumed marine fish continues to exceed human health guidelines in most marine waters. And, globally, the amount of mercury released to the environment each year from human activities is on the rise.”(13)


For additional specific evidence about harmful effects of mercury, including a 2015 finding that developmental exposure to mercury was associated with a 3-fold increase in performance below the established cut-off for borderline intellectual disability…”  at exposure levels found in part of the American population, go to the Appendix.



Section B:  Special vulnerability of infants to effects of mercury during the early postnatal period:


The highly-published expert, P. Grandjean, in an article in the American Journal of Epidemiology states:  “The nervous system is particularly vulnerable to effects from neurotoxicants such as methylmercury during the last two trimesters of pregnancy and during early postnatal life.”23  The U.S. Agency for Toxic Substances and Disease Registry (ATSDR), in its document “Mercury,” in the section (2.6) on “Children’s Susceptibility,” states that “There are critical periods of structural and functional development during both pre-natal and post-natal life and a particular structure or function will be most sensitive to disruption during its critical period(s). Damage may not be evident until a later stage of development.”40  According to the EPA, “There is general agreement that the nervous system continues development in post-natal life and that methylmercury can adversely affect the developmental processes.”25a


A 2006 study determined that, of the three sources of infant mercury exposure, ingestion (breast milk), inhalation, and dermal exposure, the largest contribution was from breast milk, providing 96 to 99.6% of the total exposure.43 


In addition to being four times the legal limit that applies to U.S. bottled water, typical mercury in breast milk is eight times the WHO relatively-safe guideline value for drinking water. 17    And many women have much higher concentrations than those typical levels.  What becomes of the mercury in women’s bodies (how heavily infants could be affected by it) is worth considering: 

-- a 1998 German study found that concentrations of mercury in breast milk of 85 lactating women at two months after birth had declined by an average of over 70% from their levels at time of birth;24

-- According to researchers contracted by the EPA, "a wealth of information" indicates that lactational transfer of maternal mercury during the first 15 days of lactation is equal to about a third of the total transfer of mercury that takes place during gestation.25

-- According to the EPA directly, “Lactating women have shorter biological half-lives for methylmercury (average value 42 days), compared with nonlactating women (average value 79 days) (Greenwood et al., 1978). This is presumably a reflection of excretion of mercury into milk.” 25a

-- a 2007 study of 82 mother-infant pairs found that mercury levels in mothers’ hair decreased 57% during six months of lactation;26

-- According to a 1999 Swedish study, “there was a marked decrease in I-Hg (inorganic mercury) in (the mothers’) blood and urine during lactation, most likely related to the excretion of I-Hg in milk…. About 10% of the Hg (mercury) present in circulating blood (5 L]0.3 lg/L) would be transferred to the milk every day.”27   (Obviously, the mother also keeps taking in mercury.)

 -- In a study by a prominent scientist (P. Grandjean) and his team, it was found that total mercury concentrations in infants that had been breastfed for one year were three times as high as those in infants that had not been breastfed.(27c) 

--  Another study found more than doubling of infant mercury levels due to 6 months of breastfeeding.(27d)

-- Evidence from the Iraqi poisoning incident showed that lactation decreased blood mercury clearance half-times in women by 44%.(27a)

-- The average whole body biological half-life of inhaled mercury is approximately 60 days, but it is estimated that the half-life of mercury in the brain can be as long as 20 years.27e  The above findings of doubling and tripling of mercury levels in breastfed infants would have been based on levels in the whole body, where half-lives are relatively short and accumulation relatively minor, as opposed to levels in the especially vulnerable developing brain, where accumulation would be far greater.


In addition to infants’ high ingestion of mercury via breastfeeding, absorption of mercury also appears to be high while the infant is on a milk-based diet, as indicated in an experiment with monkeys.(27b)



Section C:  Specifics about damage caused by mercury, especially as related to autism:

Based on considerable earlier research, a 2013 study in the National Library of Medicine generalized, “the cerebellum has emerged as a region of interest in autism studies because of converging findings from human postmortem research, human neuroimaging studies, and animal models…. Evidence appears to support cerebellar dysfunction…as a contributor to the autism phenotype.”28   In relation to that, according to the ATSDR, “the predominant neuropathological feature (of effects of methylmercury exposure) is degenerative changes in the cerebellum.29  As mentioned earlier, many studies have found high mercury levels in those diagnosed with autism, including evidence of unusually high exposure during the neurodevelopmentally vulnerable period of infancy.7, 7b  



Figures 1 and 2

The EPA-contracted research group referred to earlier provides good reason to be especially concerned about postnatal infant ingestion of mercury, which is that "the brain is especially vulnerable (to metals) during the brain growth spurt."(30)  Notice in the chart above left that most of the brain growth spurt, especially in the cerebellum, takes place in the year after birth.  And note that this period of maximum vulnerability to metals occurs at the same time as a breastfed infant is ingesting a surge of mercury that will transfer to the infant much or most of a grown person’s accumulation of that toxin. (see Section B above)  And remember from the previous paragraph the close connection between cerebellar dysfunction and autism, as well as the harmful effect of methylmercury on the cerebellum.


While noting in this chart the major amount of growth of the brain taking place postnatally, note that tissues undergoing growth (to which cell division is important) are especially vulnerable to methylmercury, since “methylmercury is known to inhibit cell division by causing metaphase arrest,” according to a WHO publication (31)


There are many close similarities between known effects of mercury and traits of ASD (autism spectrum disorders).  Those include (a) mercury’s known latency (of months to years) after exposure before effects become apparent, which is relevant to autism’s pattern of late emergence and/or regression (see Section F), (b) abnormal social behavior, and (c) many others, which can be read about in section 5.b of


Timing of the brain’s maximum general vulnerability to toxins is important:   According to EPA researchers, an organ is generally at its greatest vulnerability to environmental toxicants if exposure to the toxins occurs during development of that organ.32   Note in the above chart the similarity between the period of the greatest amount of growth of the brain and the period of breastfeeding. Note also in Figure 2 the specific functions’ connections that are developing in the brain after birth, which developments are therefore vulnerable to toxins after birth, functions that are related to disabilities that have been greatly increasing in recent decades. For details on this subject, see


Another study also found adverse cognitive effects of postnatal methylmercury levels, measured well past the prenatal period, in toddlers.   After adjustment for fish intake, T-Hg levels (total mercury levels) (in hair) > or =1 microg/g were associated with decrements in the general cognitive (-6.6 points), memory (-8.4 points), and verbal (-7.5 points) MSCA scores.”32b  This amount of exposure corresponded to the EPA’s Reference Dose,32c not an especially high exposure.


Laboratory experiments with animals are widely conducted to find effects of various potential toxins on the brain, under carefully-controlled conditions.  An experiment with prairie voles (which have similarities to humans in social interaction) found that chronic ingestion of mercury in environmentally-relevant doses substantially reduced social contact by male voles when they were given a choice between isolation or contact with an unfamiliar same-sex mole. The effects of metals ingestion were specific to males: no effects of metals exposure were seen in females.  The authors concluded, “thus, an ecologically relevant stimulus (mercury ingestion) produced two of the hallmark characteristics of autism – social avoidance and a male-oriented bias…..”32a


Although most of this article deals with mercury and its effects, it should also be pointed out that there are other important toxins that could also be contributing to problems in neurological development of infants.  Some that stand out are dioxins (including their chemical relatives, PCBs) and PBDEs; those appear to be the only other developmental toxins besides mercury that are known to be ingested in concentrations that greatly exceed established safe levels in typical human milk. (See  As indicated at that website, with authoritative sources, most of those toxins (including mercury) are present in infant formula in concentrations less than 2% as high, and usually less than 1% as high, as in human milk.



Section D:  Alternative types of infant nutrition, with different concentrations of mercury:


Some may wonder why human milk should be so much higher in mercury than cows’ milk or infant formula.  Aside from fish and other seafood, the principal source of mercury in typical human bodies is absorption of matter originating from dental amalgam, which is about 50% mercury.  As mentioned earlier, there are other sources that especially affect many mothers, including residence near municipal or hospital waste incinerators, being near diesel emissions or high vehicle traffic, working with certain art materials or in dental offices or some laboratories, use of certain cosmetics, being inside buildings with certain kinds of paint, etc.  It should therefore not be surprising that products of cows and soybean fields do not have the mercury concentrations that are found in human milk. The only readily-found survey of mercury in infant formula products (in Canada, 2003) found the average mercury level in milk-based, ready-to-use formula to be 0.028 ng/g (=.028 billionths of a gram per gram, or 0.028 ppb).33  This is well below one percent of the mercury concentration in average breast milk, going by the best available data as quoted above.  In addition:  A study (Hapke, 1991) found that “cattle are able to demethylate mercury in the rumen and thus absorb less mercury.”



Section E:  Other questions about effects of mercury exposure in the early postnatal period:


The question is also likely to come up as to why serious effects of postnatal exposure to mercury should be found, considering the widespread impression that neurodevelopmental harm resulting from toxins is likely to occur from prenatal exposures.  The answer to that question is somewhat lengthy and is presented with citations of authoritative sources at; a few of the points presented there include the recognition by many experts and health-related government agencies of harmful effects of postnatal exposures to toxins, the tremendous increases in exposures to toxins postnatally compared with prenatal exposures, the large number of published studies that have found neuro-developmental harm to result from specifically postnatal exposures, and explanation of how incorrect impressions grow.  For a detailed statement on the above subject, go to the above link.


Another logical question is, why should levels of mercury and other toxins in breast milk be a source of developmental harm these days when they weren’t in earlier times?  Aside from exposures to mercury via dental amalgam, by far the largest proportions of human exposures to these toxins in the environment originate as products of modern combustion (of fossil fuels) and industrial processes.  Mercury is naturally present in the environment, but humans receive little exposure to it except from sources that originate from modern human activity.  Mercury emitted by coal-fired power plants drifts for thousands of miles and settles into bodies of water, where it builds up in the tissues of fish and seafood, reaching much higher levels in larger fish that are higher up in the aquatic food chain, thereby becoming the other major source of mercury in humans.  Despite efforts by the EPA, mercury in the environment has only been increasing at a less rapid pace than otherwise.  According to a document on mercury of the U.S. Agency for Toxic Substances and Disease Registry on their website in December of 2014, “environmental levels of mercury are continuing to rise.”(33a)



One implication of the above is that, if we want to avoid transferring the most harmful doses of toxins to infants, we should seek to minimize the postnatal transfers. The most effective way to do that would be to depart from the breastfeeding recommendations that have been increasingly followed in recent decades.  But those policies have considerable support in the population and among doctors. However, there are additional good reasons for reconsidering those recommendations:


-- High infant exposures to serious developmental toxins could be avoided by means of parents’ reverting to bottle feeding of infants, which was the predominant feeding type in the mid-20th century,35 without negative health effects being apparent as of a half-century later. (See below for comparisons with later periods.)


 -- Four decades of historical child health data (mainly from the CDC) have shown that the major increases in breastfeeding rates since 1971 have been followed by substantial increases in all but one of the disorders that are alleged by the U.S. Surgeon General to be reduced by breastfeeding.36


-- Epidemics and increases of other childhood disorders (diabetes, asthma, allergies, obesity, ADHD and apparently mental retardation and autism) came about following the transition from low to high breastfeeding rates.37


-- Good reason to see a reversion to mainly bottle-feeding as a reasonable alternative, compared with the type of infant feeding that is high in known neuro-developmental toxins, can be found in

-- the historical record (see above),

-- the 50+ studies that have found adverse effects of breastfeeding,38 and

-- the increasingly wide acceptance of the “hygiene hypothesis” as an explanation for the increases in immunity-related diseases (including asthma, allergies and type 1 diabetes) among children;39 according to this hypothesis, microbial exposure in contemporary developed countries is already too low to provide the needed stimulus for proper development of children’s immune systems, due to increases in hygiene in recent times; the additional shielding of infants from microbes as provided by the immune cells in breast milk should be seen in that light.




It is interesting to note the results of another study of effects of mercury that was carried out in the Seychelles (Davidson et al., 201039a), as follows: 

 Fig. 3

Investigating children exposed to mercury by way of high seafood consumption, it was found that prenatal exposures had no significant effects, but postnatal exposures did appear to have substantial adverse effects on male children when tested at ages 9 and 17. (See charts.)



On the left are large sections of Figures 1 and 2 from the above-mentioned study, showing results for a number of different scholastic achievement tests administered to children who had varying levels of mercury.  Shown on the left are all of the charts in which results were indicated separately by gender.  The tests that were not broken down by gender showed no consistent associations of mercury with achievement, in contrast with the results that were shown separately for males and females, in these charts. 


The above contrasting effects of mercury on males versus females is especially noteworthy because of its probable relevance to both autism and ADHD, both of which affect males predominantly.



Section F:  Long-term, latent neurotoxic effects of mercury exposure

An official document of the EPA presents two paragraphs summarizing many scientific findings about delayed neurotoxic effects of methylmercury; in addition to observations of delayed effects in humans, this document reports that “Animal studies lend support to the conclusion that methylmercury can have delayed effects that are uncovered with age.”  It concludes, “All of these observations are consistent with a hypothesis that either developmental or adult exposure to methylmercury can have adverse long-term sequelae that may not be detected for years or decades following cessation of exposure.39b  There is considerable evidence supporting this generalization.39c  Remember the ATSDR statement in Section B that “Damage (from developmental exposure to mercury) may not be evident until a later stage of development.” 40 This should be seen in relation to the frequent occurrence of regression or late emergence of characteristics of ASD.  It is also relevant to the serious problems of mental incapacity, including Alzheimer’s and dementia, and the growing expenses to society of caring for those affected, as people live longer than in earlier generations.




Comments or questions are invited.  At the next link are comments and questions from readers, including a number of doctors.  Some of the doctors have been critical but at least four have been in agreement with us, including two with children of their own with health problems and one who says she has delivered thousands of babies; they put into briefer, everyday language and personal terms some important points that tend to be immersed in detail when presented in our own publications.  Also, we have responded to many readers’ questions and comments, including about having breast milk tested for toxins and about means of trying to achieve milk that is relatively free of toxins, including the “pump and dump” option.  To read the above, with a link for sending your own comments or questions, go to   If you have criticisms, please be specific about any apparent inaccuracies, rather than merely saying you don’t like what is said here.  Note that we don’t feel obligated to present the favorable side of the breastfeeding debate, since that is already very amply (and one-sidedly) presented in many other, widely-distributed publications as well as in person by numerous enthusiastic promoters. 


* To read about the author of this article, go to the end after the footnotes.




Appendix:  More evidence about effects of Methylmercury:

-- Methylmercury is one of the “environmental agents with the property of killing neurons as they are born,” according to a study referred to by the NIH.44   

-- Rats exposed to methylmercury on postnatal day 7 were found to have brain cell death induced by one exposure to methylmercury at a level “that begins to approximate human exposure;” and this dose was “equivalent to a single daily exposure” at a level that is estimated to be chronic for many humans.45    

-- Methylmercury accumulates in the brain, and has been found to reach levels over seven times the levels in the blood.46, 47   

-- The U.S. Agency for Toxic Substances and Disease Registry (ATSDR) refers to “deranged neuronal cell migration” that may result from the developing nervous system’s exposure to methylmercury, during particularly sensitive periods of children’s neurological development occurring in the early months after birth as well as prenatally.48   

--  According to an EPA report to Congress, Neuronal migration, a process specifically affected by methylmercury, begins at about six weeks in utero, and the process continues until five months after birth (Chi et al., 1977)….  Considering the broad-based impairment of nervous system metabolism that can be produced by methylmercury…, that nervous system development continues postnatally through at least the third to fourth year of life.”49

-- A study in the San Francisco Bay area found that atmospheric exposures to metals, especially mercury, were associated with autism prevalence.53


-- A major 2014 review article reported as follows:  “Another ecological study in Texas (aside from the Palmer et al. study that has received valid criticism) reported that the residential distances to industrial or power plant (P<0.05 for both) sources of mercury (estimated from the US EPA Toxic Release Inventory) were independently correlated with autistic disorder prevalence such that prevalence increased exponentially with increasing proximity to mercury sources.47” (in #52 here). “In another study from Texas and California, the prevalence of autism was significantly greater (P=0.01 for Texas; P=0.04 for California) in geographical areas that had the highest concentrations of ambient mercury. In addition, a significant correlation was observed between the mercury concentration in ambient air and the autism prevalence by state.48 (in #52 here)


Continuing from that same review article, ASD prevalence was significantly correlated with mercury and lead environmental atmospheric concentrations in another study using Combinatorial Fusion Analysis and Association Rule Mining.49(in #52 here)  The prevalence of ASD for 59 parishes in Louisiana, as obtained from the Louisiana Department of Education, significantly correlated (P<0.001) with the mercury concentrations of 7652 fish samples measured throughout the state by the Louisiana Department of Environmental Quality in another study.50 (in #52 here)  Finally, the eighth ecological study reported that fish advisories related to mercury were significantly correlated with autism prevalence for all 50 states (r=0.48, P<0.001).51 (in #52 here)  Collectively, these eight ecological studies are limited by a cross-sectional design that prevents firm conclusions on causation, but they provide evidence for an association between ASD and heavy metal exposures in the environment.(52) 


The authors of a study published in 2015 study stated that their investigation confirmed associations of mercury exposure with “poorer cognitive function in school-age children reported in the Faroe Islands,” as well as reporting “an association with school-age IQ.”  Continuing, “the more heavily exposed children had a 3-fold increased likelihood of falling within the borderline range for intellectual disability on school-age IQ,….  Thus, these data… indicate that it (mercury) is associated with clinically meaningful impairment in overall cognitive function at levels of exposure within the range found in the general U.S. population.”  The authors cited three other studies in support of their statement, Mercury impairs cognitive development.”54  Those authors used the term “prenatal” to refer to mercury levels measured in umbilical cord blood in their study, without explaining why those measurements would not also be indicative of postnatal infant exposures to mercury that take place via breastfeeding, while the growing brain continues to be developmentally vulnerable.


*To read about Pollution Action and the author of this article, go to




     1) National Scientific Council on the Developing Child, Early Exposure to Toxic Substances Damages Brain Architecture, 2006, p. 3, at


1a)  A publication of the Executive Director of the Center for Sensorimotor Neural Engineering at the University of Washington refers to a five-fold increase in formation of synapses postnatally compared with prenatally. (Chudler, Brain Plasticity -- What is It? at,  citing Gopnic, A., Meltzoff, A., Kuhl, P. (1999). The Scientist in the Crib: What Early Learning Tells Us About the Mind, New York, NY: HarperCollins Publishers) 

It appears to be very widely accepted thatDuring the first three years of life in humans, there is a period of rapid synapse formation that connects nerve cells into functioning circuits. This time of rapid synapse formation is the critical period in brain development.(28d) (Emphasis on “the” is in the original.)  The New York Times writer just quoted (who for eighteen years had been following research and awarding grants in education, cognitive psychology, and neuroscience at three foundations) apparently sees no disagreement about the existence of the birth-to-age-three “early stage of exuberant synapse formation.”  (John T. Bruer, “The Myth of the First Three Years: A New Understanding of Early Brain Development and Lifelong Learning,” in NY Times Books section at

See also Tau et al., Normal Development of Brain Circuits, Neuropsychopharmacology. Jan 2010; 35(1): 147–168. Published online Sep 30, 2009. doi:  10.1038/npp.2009.115  at


2) EPA web page at concerning exposure source;  Agency for Toxic Substances and Disease Registry web page at


3) Grandjean et al., Methylmercury and brain development:  imprecision and underestimation of developmental neurotoxicity in humans.  Mt Sinai J Med. 2011 Jan-Feb;78(1):107-18. doi: 10.1002/msj.20228.  at 


3a) The National Academies Press,  Toxicological Effects of Methylmercury (2000) at   Discussing the effects of “chronic, low-dose prenatal MeHg exposure from maternal consumption of fish”  (p.4),..  “there is a large body of scientific evidence showing adverse neurodevelopmental effects, including well-designed epidemiological studies.” (p. 6)


4) Koren et al., Fish consumption in pregnancy and fetal risks of methylmercury toxicity, Can Fam Physician. Oct 2010; 56(10): 1001–1002.  PMCID: PMC2954077 at


4b) Center on the Developing Child at Harvard University, National Scientific Council on the Developing Child:  Early Exposure to Toxic Substances Damages Brain Architecture, 2006, Working Paper No. 4; especially introduction, pp. 2, 7, 9;  link for this publication at  This Council is comprised of twelve leading scholars from all over the U.S.


5) For another review article on the subject, see Yoshimasu et al., A meta-analysis of the evidence on the impact of prenatal and early infancy exposures to mercury on autism and attention deficit/hyperactivity disorder in the childhood, Neurotoxicology, 2014 Sep;44:121-31. doi: 10.1016/j.neuro.2014.06.007. Epub 2014 Jun 19, at

Studies with similar findings from other countries can be found by doing a search with the phrase “maternal methylmercury effects on children,” at


6) U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury,  at, Section, p. 146


6a) Figure 1 of Mahaffey et al., Blood Organic Mercury and Dietary Mercury Intake: National Health and Nutrition Examination Survey, 1999 and 2000, Environmental Health Perspectives, volume 112 | number 5 | April 2004 •  at


6b) Mahaffey et al., Blood organic mercury and dietary mercury intake: National Health and Nutrition Examination Survey, 1999 and 2000, Environ Health Perspect. <#> 2004 Apr;112(5)


7)  Geier DA et al., Blood mercury levels in autism spectrum disorder: Is there a threshold level?  Acta Neurobiol Exp (Wars). 2010;70(2):177-86,    Also see footnotes 6, 15, 16, and 29  in D. Austin, An epidemiological analysis of the ‘autism as mercury poisoning’ hypothesis’, International Journal of Risk and Safety in Medicine, 20 (2008) 135-142  at; Priya et al., 2011, 1999a. Toxicological Profile for MercuryLevel of trace elements (copper, zinc, magnesium and selenium) and toxic elements (lead and mercury) in the hair and nail of children with autism. Biol Trace Elem Res. 2011;142:148–158;  Hassanien et al., Environmental Heavy Metals and Mental Disorders of Children in Developing Countries. Environm Risk. 2011;1:1–25.;. El-Baz et al., Hair Mercury Measurement in Egyptian Autistic Children. Egypt J Med Human Gen. 2010;11:135–141; Al-Farsi et al., Levels of heavy metals and essential minerals in hair samples of children with autism in Oman: a case-control study (2013)


7a) Adams et al., Toxicological status of children with autism vs. neurotypical children and the association with autism severity, Biol Trace Elem Res. 2013 Feb;151(2):171-80. doi: 10.1007/s12011-012-9551-1. Epub 2012 Nov


Also see Adams and 11 others: The Severity of Autism Is Associated with Toxic Metal Body Burden and Red Blood Cell Glutathione LevelsJ Toxicol. 2009; 2009: 532640. , PMCID: PMC2809421 at

7b)  Adams et al., Mercury, lead, and zinc in baby teeth of children with autism versus controls, J Toxicol Environ Health A., 2007 Jun;70(12)

7c) see


8) Code of Federal Regulations, Title 21, Chapter 1, Subchapter B, Part 165, Subpart B, Sec. 165-110 at


9). U.S. ATSDR document on mercury at, p. 443


10)  2004 International Emissions Inventory Conference, Air Toxics Session, Clearwater, Florida, Mercury Emissions from Motor Vehicles, at

        Also,  Hoyer et al., Mercury Emissions from Motor Vehicles (EPA publication), esp. p 4, at


      11) Roberts et al., Perinatal Air Pollutant Exposures and Autism Spectrum Disorder in the Children of Nurses’ Health Study II Participants, published June, 2013 in Environmental Health Perspectives, at


12) Solomon et al., Chemical Contaminants in Breast Milk: Time Trends and Regional Variability, Environmental Health Perspectives • Volume 110 | Number 6 | June 2002 at


13)  Sources to Seafood: Mercury Pollution in the Marine Environment, The Coastal and Marine Mercury Ecosystem Research Collaborative (C-MERC) Coordinated by Dartmouth College Toxic Metals Superfund Research Program, November 30, 2012, at


17)  Mercury is typically present at 8 parts per billion in breast milk, according to U.S. ATSDR document on mercury at, p. 443,  which compares with1 microgram per liter (1 microgram per billion micrograms), or 1 part per billion, the WHO guideline value for drinking water:  (WHO, Mercury in Drinking-water Background document for development of WHO Guidelines for Drinking-water Quality  WHO/SDE/WSH/03.04/10  at  p. 8   Accessed 4/8/2014)


22) Essex et al., Breastfeeding rates in New Zealand in the first 6 months and the reasons for stopping. N Z Med J. 1995 Sep 8;108(1007):355-7.  at, showing a 94% exclusive breastfeeding rate at birth in a study published in 1995. Breastfeeding rates as of 2012 were higher than in 1995.  (  Also National Breastfeeding Advisory Committee of New Zealand’s advice to the Director-General of Health, National Strategic Plan of Action for Breastfeeding 2008–2012,  at


23) P. Grandjean,  Methylmercury Exposure Biomarkers as Indicators of Neurotoxicity in Children Aged 7 Years,  American Journal of Epidemiology 1999,  The Johns Hopkins University School of Hygiene and Public Health  at


24) Drexler et al., The mercury concentration in breast milk resulting from amalgam fillings and dietary habits,  Environ Res. 1998 May;77(2):124-9. at  The concentrations were also positively associated with fish consumption, which implies that a high percentage of the mercury in the breast milk was in the form of methylmercury, which is the most toxic form and the form chiefly present in fish;   another study found various forms of mercury in mothers’ blood and urine declined during lactation, and said that was probably attributable to excretion during breastfeeding. (Vahter, Longitudinal Study of Methylmercury and Inorganic Mercury in Blood and Urine of Pregnant and Lactating Women, as Well as in Umbilical Cord Blood, Environmental Research, Volume 84, Issue 2, October 2000, Pages 186–194


25) Exploration of Perinatal Pharmacokinetic Issues  Contract No. 68-C-99-238, Task Order No. 13  Prepared for EPA by: Versar, Inc. EPA/630/R-01/004, Section,  at  

The highly effective transfer of mercury from mother to infant via breastfeeding is also compatible with the finding that the half-life of methylmercury in the blood of lactating women is about half that in nonlactating women, due to excretion in breast milk. (Wigle, D.T., MD, PhD, MPH:  Child Health and the Environment, Oxford University Press, 2003, Ch. 5. p. 106, typically available through Ebsco Host at local libraries)


25a) Mercury Study Report to Congress c7o032-1-1,  Office of Air Quality Planning & Standards and Office of Research and Development  Volume VII, Section,  at


26) Marques RC, et al., Hair mercury in breast-fed infants exposed to thimerosal-preserved vaccines.Eur J Pediatr. 2007 Sep;166(9):935-41. Epub 2007 Jan 20  at  


27) Vahter et al., Longitudinal Study of Methylmercury and Inorganic Mercury in Blood and Urine of Pregnant and Lactating Women, as Well as in Umbilical Cord Blood, Environmental Research, Section A 84, 186}194 (2000) at


27a)  According to the U.S. Hazardous Substances Data Bank of the National Library of Medicine's TOXNET system, at


27b) Lok, E. 1983. The effect of weaning on blood, hair, fecal and urinary mercury after chronic ingestion of methylmercuric chloride by infant monkeys. Toxicology Letters, Volume 15, Issues 2–3, February 1983, Pages 147–152, abstract at


27c)  P. Grandjean et al., Human Milk as a Source of Methylmercury Exposure in Infants,  Environmental Health Perspectives, accepted Oct. 1993

27d)  Marques RC, et al., Hair mercury in breast-fed infants exposed to thimerosal-preserved vaccines. Eur J Pediatr. 2007 Sep;166(9):935-41. Epub 2007 Jan 20  This study found that mercury measured in infants’ hair increased 446% during the first six months of breastfeeding, while mercury measured  in the mothers’ hair decreased 57%. These measurements included mercury from vaccines (still containing mercury at that time in Brazil, where the study was carried out), which the authors estimated accounted for about 40% of the infants’ exposure during those six months.  Given that, combined with the finding in a Taiwanese study that over 95% of an infant’s exposure to mercury was from breastfeeding,(43) the increase in the infants’ mercury levels attributable to breastfeeding was probably well over 200% during the first 6 months of breastfeeding.

27e) Rice et al., Environmental Mercury and Its Toxic Effects, J Prev Med Public Health. 2014 Mar; 47(2): 74–83, doi: PMCID: PMC3988285  at

28) Gadad et al., Neuropathology and Animal Models of Autism: Genetic and Environmental Factors,  Autism Res Treat.

2013; 2013: 731935 PMCID: PMC3787615   at


29) Section of U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury  at  

See also Section of International Programme On Chemical Safety,  Environmental Health Criteria 101Methylmercury  (a publication of WHO, Geneva, 1990) at

For ataxia-producing effect of methylmercury, see also p. 6-21 of U.S. EPA, Mercury Report to Congress, Vol. VII, Dec. 1997, EPA-452/R-97-009  at


30) Exploration of Perinatal Pharmacokinetic Issues  Contract No. 68-C-99-238, Task Order No. 13  Prepared for EPA by: Versar, Inc. EPA/630/R-01/004, Section,  at   See reference 17d below about mercury exposure in humans being mainly methylmercury.

The highly effective transfer of mercury from mother to infant via breastfeeding is also compatible with the finding that the half-life of methylmercury in the blood of lactating women is about half that in nonlactating women, due to excretion in breast milk. (Wigle, D.T., MD, PhD, MPH:  Child Health and the Environment, Oxford University Press, 2003, Ch. 5. p. 106, typically available through Ebsco Host at local libraries)


31) International Programme On Chemical Safety,  Environmental Health Criteria 101Methylmercury  (a publication of WHO, Geneva, 1990)  at  Sections 9.1 and 9.42


32) Rodier, “Developing Brain as a Target of Toxicity,” Environmental Health Perspectives, at


32a) Curtis et al., Chronic Metals Ingestion By Prairie Voles Produces Sex-Specific Deficits In Social Behavior: An Animal Model Of Autism, Behav Brain Res. 2010 Nov 12; 213(1): 42–49.  Published online 2010 Apr 28. doi:  10.1016/j.bbr.2010.04.028  PMCID: PMC2880538 at


32b)   Freire et al., Hair mercury levels, fish consumption, and cognitive development in preschool children from Granada, Spain,  Environ Res. 2010 Jan;110(1):96-104. doi: 10.1016/j.envres.2009.10.005   at


32c) Grandjean et al., Neurotoxicity from prenatal and postnatal exposure to methylmercury, Neurotoxicol Teratol. 2014 May-Jun; 43: 39–44. PMCID: PMC4066386  at


33).  Food Additives & Contaminants: Part B: Surveillance  Volume 5, Issue 1, 2012  Robert W. Dabeka et al., Survey of total mercury in infant formulae and oral electrolytes sold in Canada  DOI: 10.1080/19393210.2012.658087  at

33a) U.S. ATSDR, “Toxicological Profile for Mercury”, 1999, p. 355, at


34) See for a more complete statement about those toxins


35) International Programme On Chemical Safety,  Environmental Health Criteria 101Methylmercury  (a publication of WHO, Geneva, 1990)  at  Section 9.3.2


35)  American Academy of Family Physicians website at

36)  See, where numerous peer-reviewed studies are cited in support of this statement.


37) CDC’s MMWR National Surveillance for  Asthma -- United States, 1980-2004, Table 29, at

Re allergies: CDC’s Health United States 2011, Table 46, p. 3, at  

Type 2 Diabetes in Children and Young Adults:  A “New Epidemic”  Francine Ratner Kaufman, MD  CLINICAL DIABETES • Volume 20, Number 4, 2002  at 

Re ADHD:  see for substantial evidence about the time trend of ADHD in the U.S.

Re mental retardation trend: National Center for Health Statistics, Healthy People 2000 Review, 1997.  Public Health Service. Lib. of Congress Cat. No. 76-641496, Figure R, found at

Also see, where numerous peer-reviewed studies are cited in support of this statement .


38)  See, where over 50 peer-reviewed studies are cited in support of this statement.


39)  Also Clin Exp Allergy. 2006 April; 36(4): 402–425.  Blackwell Publishing Ltd  "Too clean, or not too clean: the Hygiene Hypothesis and home hygiene,"  SF Bloomfield et al.   Also Cell Research advance online publication 24 April 2012; doi: 10.1038/cr.2012.65  "Early exposure to germs and the Hygiene Hypothesis"  Dale T Umetsu  Division of Immunology, Karp Laboratories, Children's Hospital Boston, Harvard Medical School, Boston,MA

Also, "About Allergies/ Why Are Allergies Increasing?" at


39a) Davidson et al., Fish Consumption, Mercury Exposure, and Their Associations with Scholastic Achievement in the Seychelles Child Development Study, Neurotoxicology. Author manuscript; available in PMC Sep 1, 2011, Published in final edited form as:Neurotoxicology. Sep 2010; 31(5): 439–447. Published online May 31, 2010. doi:  10.1016/j.neuro.2010.05.010, PMCID: PMC2934742  at


39b) U.S. EPA’s Integrated Risk Information System web page on methylmercury (“Methylmercury (MeHg) (CASRN 22967-92-6)) at, using their “Search IRIS” for methylmercury.


39c) Adams et al., Workshop to Identify Critical Windows of Exposure for Children's Health:  Neurobehavioral Work Group Summary, Environmental Health Perspectives * Vol 108, Supplement 3 * June 2000, at


40) Section 2.6 of U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury, p. 301  at


43) Chien LC, et al., Analysis of the health risk of exposure to breast milk mercury in infants in Taiwan. Chemosphere. 2006 Jun;64(1):79-85. Epub 2006 Jan 25 at 


44) Rodier, “Developing Brain as a Target of Toxicity,” Environmental Health Perspectives, at

45) Sokolowski et al., Methylmercury (MeHg) elicits mitochondrial-dependent apoptosis in developing hippocampus and acts at low exposures, Neurotoxicology  2011  at 

46)  U.S. Agency for Toxic Substances and Disease Registry web page at, saying "Methyl mercury is the most toxicological form of the element and, by its accumulation in the central nervous system (CNS), may result in neurotoxic effects…."

 Also Berlin M. 1979. Mercury. Handbook on the Toxicology of Metals. Amsterdam: Elsevier.


      47) Burbacher et al., Comparison of Blood and Brain Mercury Levels in Infant Monkeys Exposed to Methylmercury or Vaccines Containing Thimerosal,  (Oral Mg Kinetics section)  Environ Health Perspect. 2005 August; 113(8): 1015–1021, PMCID: PMC1280342  at


48) U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury  at,  p. 214 re “deranged” neuronal migration.  Also Section 1.6 re particularly sensitive periods of neurological development.


49)  EPA-452/R-97-009 December 1997  p. 5-29 (Section 5.6.1) at


52)  Rossignol et al., Environmental toxicants and autism spectrum disorders: a systematic review, Transl Psychiatry. 2014 Feb; 4(2): e360. PMCID: PMC3944636  at


53) Windham et al., Autism Spectrum Disorders in Relation to Distribution of Hazardous Air Pollutants in the San Francisco Bay Area, Environ Health Perspect. 2006 Sep; 114(9): 1438–1444. Published online 2006 Jun 21. doi:  10.1289/ehp.9120 PMCID: PMC1570060 at


54) Jacobson et al., Relation of Prenatal Methylmercury Exposure from Environmental Sources to Childhood IQ, Environ Health Perspect; DOI:10.1289/ehp.1408554 , Volume 123 | Issue 8 | August 2015 at





See also: 


Grandjean et al., Human Milk as a Source of Methylmercury Exposure in Infants,  Environ. Health Perspectives, accepted Oct. 1993  


Weiss et al., Silent Latency Periods in Methylmercury Poisoning and in Neurodegenerative Disease, Environmental Health Perspectives • Volume 110 | Supplement 5 | October 2002 at



    also  Mendola  P et al, Environmental factors associated with a spectrum of neurodevelopmental deficits, Ment Retard Dev Disabil Res Rev. 2002;8(3):188-97  abstract at or full text  at


   Also, P. Grandjean,  Methylmercury Exposure Biomarkers as Indicators of Neurotoxicity in Children Aged 7 Years,  American Journal of Epidemiology 1999,  The Johns Hopkins University School of

Hygiene and Public Health  at


U.S. ATSDR, Public Health Service, Toxicological Profile for Mercury 






*As the author of the above, my role has not been to carry out original research, but instead it has been to read through very large amounts of scientific research that has already been completed on the subjects of environmental toxins and infant development, and then to summarize the relevant findings; my aim has been to put this information into a form that enables readers to make better-informed decisions related to these matters.  The original research articles and government reports on this subject (my sources) are extremely numerous, often very lengthy, and usually written in a form and stored in locations such that the general public is normally unable to learn from them. 



My main qualification for writing these publications is ability to find and pull together large amounts of scientific evidence from authoritative sources and to condense the most significant parts into a form that is reasonably understandable to the general public, while maintaining accuracy in what is said.  My educational background included challenging courses in biology and chemistry in which I did very well, but at least as important has been an ability to correctly summarize in plain English large amounts of scientific material.  I scored in the top one percent in standardized tests in high school, graduated cum laude from Oberlin College, and stood in the top third of my class at Harvard Business School.  



There were important aspects of the business school case-study method that have been helpful in making my work more useful than much or most of what has been written on this subject, as follows:   After carefully studying large amounts of printed matter on a subject, one is expected to come up with well-considered recommendations that can be defended against criticisms from all directions.  The expected criticisms ingrain the habits of (a) maintaining accuracy in what one says, and (b) not making recommendations unless one can support them with good evidence and logical reasoning.  Established policies receive little respect if they can’t be well supported as part of a free give-and-take of conflicting evidence and reasoning.  That approach is especially relevant to the position statements on breastfeeding of the American Academy of Pediatrics and the American Academy of Family Physicians, which statements cite only evidence that has been

   (a) selected, while in no way acknowledging the considerable contrary evidence and a1

    (b) of a kind that has been authoritatively determined to be of low quality;a1a former U.S. Surgeon General Regina Benjamin acknowledged that essentially all of the research supporting benefits of breastfeeding consists merely of observational studies.  One determination that evidence from observational studies is of low quality has been provided by Dr. Gordon Guyatt and an international team of 14 associates;a2 Dr. Guyatt is chief editor of the American Medical Association’s  Manual for Evidence-based Clinical Practice, in which 26 pages are devoted to examples of studies (most of which were observational) that were later refuted by high-quality studies.a2a  A similar assessment of the low quality of evidence from observational studies has been provided by the other chief authority on medical evidence (Dr. David Sackett),a2c  writing about “the disastrous inadequacy of lesser evidence,” in reference to findings from observational studies.a2b


When a brief summary of material that conflicts with their breastfeeding positions is repeatedly presented to the physicians’ associations, along with a question or two about the basis for their breastfeeding recommendations, those associations never respond.  That says a great deal about how well their positions on breastfeeding can stand up to scrutiny.


The credibility of the contents of the above article is based on the authoritative sources that are referred to in the footnotes:  The sources are mainly U.S. government health-related agencies and reputable academic researchers (typically highly-published authors) writing in peer-reviewed journals; those sources are essentially always referred to in footnotes that follow anything that is said in the text that is not common knowledge.  In most cases a link is provided that allows easy referral to the original source(s) of the information.  If there is not a working link, you can normally use your cursor to select a non-working link or the title of the document, then copy it (control - c usually does that), then “paste” it (control - v) into an open slot at the top of your browser, for taking you to the website where the original, authoritative source of the information can be found.  


The reader is strongly encouraged to check the source(s) regarding anything he or she reads here that seems to be questionable, and to notify me of anything said in the text that does not seem to accurately represent what was said by the original source.  Write to  I will quickly correct anything found to be inaccurate.


For a more complete statement about the author and Pollution Action, please go to


Don Meulenberg

Fredericksburg, VA, USA


a1) See and


a1a) The Surgeon General’s Call to Action to Support Breastfeeding 2011, p. 33, at

a2) Figure 2 in Guyatt et al., GRADE guidelines:  1. Introduction -- GRADE evidence profiles and summary of findings tables, Journal of Clinical Epidemiology, at


a2a) Dr. Gordon Guyatt is chief editor of User’s Guides to the Medical Literature:  A Manual for Evidence-based Clinical Practice, 2nd Edition (3rd is upcoming), copyright  American Medical Association, published by McGraw Hill.


a2b) Writing in The Canadian Medical Association Journal, as quoted in “Do We Really Know What Makes Us Healthy?” New York Times, published: September 16, 2007  at


a2c) In a review in the Journal of the Medical Library Association, only two guides are recommended for use by physicians in evaluating evidence in medical literature, one of which is the one edited by Guyatt et al., already referred to, and the other of which is by Dr. Sackett. (Journal of the Medical Library Association, Oct. 2002, User’s Guide to the Medical Literature:  A Manual for Evidence-Based Clinical Practice, Review by Rebecca Graves, at httpi://